The FASEB Journal • Research Communication
Simulated microgravity-induced mitochondrial dysfunction in rat cerebral arteries Ran Zhang,*,1 Hai-Hong Ran,†,1 Li-Li Cai,‡,1 Li Zhu,储 Jun-Fang Sun,* Liang Peng,* Xiao-Juan Liu,* Lan-Ning Zhang,* Zhou Fang,* Yong-Yan Fan,* and Geng Cui§,1,2 *Institute of Geriatric Cardiology, †Department of Geriatric Hematology, ‡Department of Clinical Laboratory Medicine, and §Department of Osteology, Chinese People’s Liberation Army General Hospital, Beijing, China; and 储Changhai Hospital, Second Military Medical University, Shanghai, China Exposure to microgravity results in cardiovascular deconditioning, and cerebrovascular oxidative stress injury has been suggested to occur. To elucidate the mechanism for this condition, we investigated whether simulated microgravity induces mitochondrial dysfunction in rat arteries. Four-week hindlimb unweighting (HU) was used to simulate microgravity in rats. Mitochondrial reactive oxygen species (ROS), mitochondrial membrane potential (⌬m), mitochondrial permeability transition pore (mPTP) opening, mitochondrial respiratory control ratio (RCR), MnSOD/GPx activity and expression, and mitochondrial malondialdehyde (MDA) were examined in rat cerebral and mesenteric VSMCs. Compared with the control rats, mitochondrial ROS levels, mPTP opening, and MDA content increased significantly (P
Simulated microgravity-induced mitochondrial dysfunction in rat cerebral arteries Ran Zhang,*,1 Hai-Hong Ran,†,1 Li-Li Cai,‡,1 Li Zhu,储 Jun-Fang Sun,* Liang Peng,* Xiao-Juan Liu,* Lan-Ning Zhang,* Zhou Fang,* Yong-Yan Fan,* and Geng Cui§,1,2 *Institute of Geriatric Cardiology, †Department of Geriatric Hematology, ‡Department of Clinical Laboratory Medicine, and §Department of Osteology, Chinese People’s Liberation Army General Hospital, Beijing, China; and 储Changhai Hospital, Second Military Medical University, Shanghai, China Exposure to microgravity results in cardiovascular deconditioning, and cerebrovascular oxidative stress injury has been suggested to occur. To elucidate the mechanism for this condition, we investigated whether simulated microgravity induces mitochondrial dysfunction in rat arteries. Four-week hindlimb unweighting (HU) was used to simulate microgravity in rats. Mitochondrial reactive oxygen species (ROS), mitochondrial membrane potential (⌬m), mitochondrial permeability transition pore (mPTP) opening, mitochondrial respiratory control ratio (RCR), MnSOD/GPx activity and expression, and mitochondrial malondialdehyde (MDA) were examined in rat cerebral and mesenteric VSMCs. Compared with the control rats, mitochondrial ROS levels, mPTP opening, and MDA content increased significantly (P
